Diabetic ketoacidosis as a hallmark of autoimmune diabetes occurring after two cycles of cemiplimab
| العنوان: | Diabetic ketoacidosis as a hallmark of autoimmune diabetes occurring after two cycles of cemiplimab |
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| المؤلفون: | Nasrin Saleh Jouneghani, Constantin A Dasanu, John Phillip |
| المصدر: | Journal of Oncology Pharmacy Practice. 28:722-724 |
| بيانات النشر: | SAGE Publications, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | Blood Glucose, medicine.medical_specialty, Skin Neoplasms, Cutaneous squamous cell carcinoma, Diabetic ketoacidosis, medicine.medical_treatment, Antibodies, Monoclonal, Humanized, Gastroenterology, Diabetic Ketoacidosis, Internal medicine, Diabetes mellitus, medicine, Humans, Insulin, Pharmacology (medical), Immune Checkpoint Inhibitors, Blood glucose monitoring, medicine.diagnostic_test, business.industry, Blood Glucose Self-Monitoring, Nomogram, medicine.disease, Discontinuation, Diabetes Mellitus, Type 1, Oncology, Autoimmune diabetes, Carcinoma, Squamous Cell, business |
| الوصف: | Introduction Clinical indications of immune checkpoint inhibitors have expanded to a variety of malignancies. Nearly 50% of patients with advanced cutaneous squamous cell carcinoma, respond to the programmed-death 1 inhibitor cemiplimab. To date, insulin-dependent diabetes mellitus has been documented with the use of several immune checkpoint inhibitors but not cemiplimab. Case report We report herein the first case of a patient with cutaneous squamous cell carcinoma who developed diabetic ketoacidosis and insulin-dependent diabetes mellitus following only two cycles of cemiplimab. A score of 6 on the Naranjo nomogram makes the causality relationship between cemiplimab use and the insulin-dependent diabetes mellitus probable. Management and outcome The patient's developed diabetic ketoacidosis was managed with intravenous fluids and intravenous insulin, with a prompt resolution. Cemiplimab was discontinued, and the patient was discharged on long-acting and short-acting insulin therapy, with a follow-up with endocrinology. Discussion/conclusions The mechanism by which cemiplimab caused insulin-dependent diabetes mellitus is most likely due to lack of endogenous insulin production in the setting of immune-mediated loss of pancreatic beta-cells. Patients may benefit from fasting blood glucose monitoring and early immune checkpoint inhibitor discontinuation where elevated serum glucose is detected. |
| تدمد: | 1477-092X 1078-1552 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ffdc52c54efbad586aa62fb1d58d639cTest https://doi.org/10.1177/10781552211060523Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....ffdc52c54efbad586aa62fb1d58d639c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 1477092X 10781552 |
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